Feeding involves complex sequences of learned and innate behaviors that are variable between species. The final acts of feeding behavior, ingestion and rejection, however, are stereotyped responses that are directly triggered by taste stimuli. A given taste does not always elicit the same response be it ingestion or rejection. Rather, the stimulus-response relationships yielding these responses are modulated or regulated by signals deriving from the organism's physiological state and experience. To date, analysis of the neural control of ingestive behavior has revealed little about the neural machinery involved in the modulation of ingestive consummatory behavior. The predominant hypothesis of regulated control centered exclusively in the hypothalamus is no longer tenable --hypothalamically lesioned animals recover regulated ingestive behavior. The wealth of data generated by this single integrator model and its principle metholology--focal lesions--has tended to unnecessarily assign modulatory functions to forebrain structures. We have developed methodologies for examining the topography of ingestion and rejection responses and fluid intakes of preparations that otherwise do not eat or drink. The discriminative response capacity of the intact, chronic thalamic, chronic decerebrate and lateral hypothalmic lesioned rats has already been described. Discriminative responses to taste of decerebrates do not differ from intact rats. Furthermore, we have found that decerebrate rats appear to control their ingestive consummatory behavior as a function of hours of deprivation. While transections do eliminate many capacities, the tests we have developed are precise enough to circumvent these inabilities thus allowing us to assess the presence or absence of control mechanisms that are not necessarily inherently related to the behavioral capacity usually used to demonstrate them. The goal of the proposed experiments is to define the capacity of several neural levels of the rat brain to modify ingestive consummatory responses and preabsorptive insulin release as a function of experiential and physiological factors and in so doing examine the adequacy of a hierarchical hypothesis of ingestive control as an alternative to hypotheses that are no longer tenable.